Cardiovascular Diseases ( Cvd )

Many of the risk factors for cardiovascular disease cause problems because they lead to atherosclerosis. Atherosclerosis is the narrowing and thickening of arteries and develops for years without causing symptoms. It can happen in any part of the body. Around the heart, it is known as coronary artery disease, in the legs it is known as peripheral arterial disease. The narrowing and thickening of the arteries is due to the deposition of fatty material, cholesterol and other substances in the walls of blood vessels. The deposits are known as plaques. The rupture of a plaque can lead to stroke or a heart attack. (World Heart Federation).

There are other risk factors that affect a person’s chances of developing coronary artery disease such as obesity, high blood pressure (hypertension), diabetes, lack of regular exercise, high-fat diet, and emotional stress. These other risk factors are preventable and can be changed with daily exercise, eating healthy options, and making healthy daily choices for your heart and body.

Cardiovascular disease has reportedly been the number one disease killer for men and women in the United States of America. Every one out of four deaths is caused by heart disease in the United States alone (Centers for Diseases Control and Prevention). Heart disease refers to the different types of conditions and symptoms that can affect the one’s heart and its functions to the body (Mayo Clinic). Cardiovascular/Heart disease has many causes and conditions, prevention methods and symptoms, and treatment options.

The development of an atherosclerotic plaque is relatively a very a complicated process where Plaque rupture accounts for about 76% of fatality lead by thrombi. The evolution of atherosclerosis begins with foam cell accumulation where the macrophages accumulate within arterial wall intima, progresses to form fatty streak where further accumulation of intra and extracellular lipids, this is a potentially reversible stage (Greenland p, 2013) further atheroma/fibroatheroma forms where cholesterol and phospholipids accumulate intramurally. This is a vulnerable state as it is predisposed to spontaneous rupture by inflammation and thrombus deposition may occur. Hemodynamic changes during this stage may cause ischemia or silent infarction, if large plaque rupture total occlusion may cause myocardial infarction or sudden cardiac death. Finally a complex lesion can develop where fibro muscular tissue can be seen with repair efforts followed by repeated plaque formation, this may slowly increase in size and produce significant arterial narrowing.

Atherosclerosis, the underlying cause of coronary heart disease which can affect any artery in the body, is essentially the narrowing of arteries due to excessive build up of cholesterol-rich lipids known as plaque (Insull 2009). Once the arteries become narrow, the flow of blood will be constricted, and the amount of blood, nutrients and oxygen that are able to reach the heart are reduced. As a consequence, the heart becomes increasingly hypoxic resulting in ineffective contraction. The aftermath of narrow arteries often poses serious consequences as it has a high probability of causing heart attack, angina, or even stroke (Marieb & Hoehn 2010; Insull 2009). Despite the fact that arteries will harden naturally as people age, the rate of plaque development is determined by the number of risk factors (Insull 2009). This essay will discuss and review the procedure in which the risk factors: hypertension, abnormal level of blood lipids, and smoking took to assist in the development of atherosclerosis.

Atherosclerosis, which is a chronic inflammatory disease amongst the arteries of the human body, remains the principal cause of cardiovascular related disease (Gets, 2011). Atherosclerosis results from a complicated relationship between different factors such as lipid metabolism, blood coagulation elements, cytokines, hemodynamic stress, and behavioral risk factors. (Singla et al., 2011) The pathogenesis of atherosclerosis involves oxidative stress, endothelial dysfunction and chronic inflammation, which are initiated in response to high plasma lipid levels, especially Low Density Lipoproteins. (Yu et al., Getz., 2011) Atherosclerosis is a benefactor to the pathogenesis of myocardial and cerebral infarctions, gangrene and

Eagleton (2012) explains the pathological process inflammation has in weakening the arterial wall through the release of cellular and cytokine messengers which initiate various actions

Treating Arteriosclerosis includes lifestyle changes, for some people these changes may be the only treatment necessary. The other treatment to cure atherosclerosis is by taking medication. With both of these treatments’ plaque caused by

One source of great mortality and morbidity in Europe and North America is the cardiovascular disease, Atherosclerosis. It is recognized as a chronic inflammatory disease of the intermediate and large arteries characterized by the thickening of the arterial wall and is the primary cause of coronary and cerebrovascular heart disease (Wilson, 2005). It accounts for 4.35 million deaths in Europe and 35% death in the UK each year. Mortality rate are generally higher in men than pre-menopausal woman. Past the menopause, a woman’s risk is similar to a man’s (George and Johnston, 2010). Clinical trials have confirmed that lipid accumulation, endothelial dysfunction, cell proliferation, inflammation matrix alteration and foam cell formation are

784). The immune system attempts to attack the inflamed area in the artery with special white blood cells and “cells full of fatty nutrients, foam cells, begin to form there, too” (Sapolsky, 2004, p. 43). The white blood cells are unable to properly fight the affected area, and in turn, end up adding more substance to the build up. As this process continues, the affected area becomes inflamed and physically hardens. This produces a blockage in the artery and reduces blood flow, while also causing an increase in blood pressure. At this point of the atherosclerosis build up, many people, especially women, experience angina.

Atherosclerosis initiates when endothelium becomes damaged, allowing the low-density lipoproteins cholesterol to accumulate in artery wall.

Diseases resulting in damage to the heart, coronary blood vessels or peripheral blood vessels are collectively referred to as cardiovascular disease (CVD) which includes coronary heart disease, angina, myocardial infarction, atherosclerosis, stroke etc. CVD is the leading cause of death globally, accounting for 17.3 million or 30% of deaths worldwide in 2008. CVD rates, however, are not proportional across socioeconomic groups as 80% of CVD deaths occur in low and middle income nations. Due to the growing prevalence of diabetes and obesity, CVD is expected to result in 23.3 million deaths by 2030. The underlying cause of most cardiovascular events is Atherosclerosis, a decade long chronic inflammatory disease of large and medium sized arteries,

In most countries, Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of morbidity and mortality. Despite advances in the treatment of acute and/or chronic coronary syndrome, additional therapies are still needed to reduce the high rates of recurrent CV events. Since 19th centaury it was suspected that the pathogenesis of atherosclerosis involves process of inflammation, which has become recognized as a contributory factor in the development of ASCVD and other diverse chronic diseases. Based on the results from more than 60 prospective cohort studies, a variety of inflammatory biomarkers, like C-reactive protein (CRP), interleukin-6 (IL-6), tumour necrosis factor alpha(TNF-α),

Atherosclerosis is a major form of cardiovascular disease which occurs through a processed known as arteriosclerosis in which the arteries become clogged with plaque buildup overtime. Formation of this plaque is due to the damage of endothelial cells (inner cells) that line the walls of arteries. Damage of these cells is triggered by unhealthy practices or other conditions such as smoking, lack of exercise, hypertension, diabetes or high cholesterol levels. As a result harmful material such as fat, cholesterol, palettes and other material deposit themselves into the damaged artery wall. These materials accumulate and form plaque which becomes covered with various cells that try to repair the damaged wall. These cells encapsulate the plaque

Atherosclerosis is classified as a chronic, progressive, and multifactorial disease of moderate and large sized arteries categorised by intimal lesions called atheroma plaques that pushes into the vessel lumens. Atherosclerosis leading to coronary artery is the main cause of coronary artery disease (CAD). It is vital to appreciate the central mechanisms of atherogenesis in order to understand the adverse clinical results of Coronary Artery Disease and their ensuing management. The progression of atheroma consist of several cellular and molecular events with endothelial dysfunction, leucocyte recruitment and dispedesis, LDL transcytosis, LDL oxidation, recruitment and proliferation of smooth muscle cells, synthesis of extracellular matrix proteins, build-up of foamy macrophages as well as interplay of different cytokines. (Bisht et al, 2012).